Prostanglandins enhance spread of herpes simplex virus in cell cultures.

@article{Harbour1978ProstanglandinsES,
  title={Prostanglandins enhance spread of herpes simplex virus in cell cultures.},
  author={David A. Harbour and William Blyth and Terry J. Hill},
  journal={The Journal of general virology},
  year={1978},
  volume={41 1},
  pages={
          87-95
        }
}
Stimuli such as u.v. light or trauma which induce recurrence of herpes simplex may act by affecting virus replication in the skin. Such stimuli release pharmacologically active agents in the skin, including prostaglandins (PGs) such as PGE2. These agents, and other compounds which alter levels of adenosine cyclic monophosphate (cyclic AMP), were tested for their effect on the replication of herpes simplex virus (HSV) in Vero cells. Prostanglandin E2 (PGE2) and prostaglandin F2alpha both… Expand
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References

SHOWING 1-10 OF 21 REFERENCES
Interaction between cyclic nucleotides and herpes simplex viruses: productive infection
Infection of human fibroblasts and HEp-2 cells with herpes simplex virus type 1 (HSV-1) produced a decrease in the intracellular levels of cyclic adenosine 5'- monophosphate (cAMP) and a concomitantExpand
Reactivation of herpes simplex virus infection by ultraviolet light and possible involvement of prostaglandins.
TLDR
Immunosuppressive drugs failed to induce clinical signs of reactivation but irradiation of the skin of the originally infected ear with ultraviolet light or injection of prostaglandin E2 or PBSA into this site, caused reactivation of infection. Expand
AN ALTERNATIVE THEORY OF HERPES-SIMPLEX RECURRENCE AND A POSSIBLE ROLE FOR PROSTAGLANDINS
Reactivation of herpes-simplex is thought to require stimulation of latent virus in the sensory ganglion before the virus travels to the skin and causes a lesion. An alternative theory is proposedExpand
Acute and recurrent infection with herpes simplex virus in the mouse: a model for studying latency and recurrent disease.
TLDR
The system of ear infection in the mouse is presented as a new model for studying neurovirulence, and latent and recurrent infection with herpes simplex virus. Expand
Maintenance of latent herpetic infection: an apparent role for anti-viral IgG.
TLDR
It is demonstrated that anti-viral IgG inhibited intraneuronal viral DNA and antigen synthesis, therefore restricting the appearance of infectious virus in mice receiving the ganglionic transplant. Expand
Trauma to the skin causes recurrence of herpes simplex in the mouse.
TLDR
Mild trauma was induced in the skin of mice latently infected with herpes simplex virus type I by stripping the originally infected ear with cellophane tape and the majority of animals developed reactivated disease on some occasions when stripping was repeated at monthly intervals, according to the skin trigger theory of reactivation of herpessimplex. Expand
Permeation of dibutyryl cAMP into HeLa cells and its convesion to monobutyryl cAMP.
  • E. Kaukel, H. Hilz
  • Biology, Medicine
  • Biochemical and biophysical research communications
  • 1972
TLDR
Results indicate that the sustained hormone-like actions of DBcAMP come about mainly by a high resistance to extracellular and intracellular phosphodiesterase as well as by the enzymic conversion to MBcAMP accumulating in the cells. Expand
Latent herpes simplex virus and the nervous system,.
  • J. G. Stevens
  • Biology, Medicine
  • Current topics in microbiology and immunology
  • 1975
The natural history of herpetic disease is a most intriguing phenomenon in virology, and its definition has consumed the activities of a diverse group of individuals for the past three quarters of aExpand
Increased degradation rates of protein synthesized in hepatoma cells in the presence of amino acid analogues.
TLDR
Control experiments in which the labelling order was reversed or where the animo acid and its analogue were incubated in separate cell cultures support the conclusion that abberrant proteins are rapidly degraded in vivo. Expand
Interactions between prostaglandins and calcium: the importance of bell-shaped dose-response curves.
TLDR
A hypothesis is proposed which accounts for both plateau and bell type responses to PG-calcium interactions and leads to precise predictions which can be experimentally tested in many systems. Expand
...
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